Filed under: Heart blocks
Sorry for not posting much lately, folks! I guess I’ve just been too busy…! Anyway, hope you like this one. It was brought to me by a colleague who thought I might enjoy it. He was perfectly right about that!
The patient: Elderly male, admitted to the CCU for near syncopes and episodic dizziness. He had a known atrial flutter, and was using betablockers and flecainide. I’m afraid I do not have the full list here, nor the dosages. He was sleeping when this episode occured and didn’t notice anything. He also did not pass out.
EKG description: This is atrial flutter (type 1, counter-clockwise) at approx. 260 bpm, with a high and quite varied degree of atrioventricular block. The lowest F-wave/QRS ratio in the top strip, is 4:1, resulting in a ventricular rate of around 65 bpm. Medications might play a part here, but one would suspect the ratio to be lower at this atrial rate. The long blocked period shows ventricular standstill that lasts for almost 6 seconds. This is of course the reason for his episodic dizziness and near syncopes (I’m surprised he didn’t syncope completely). In the lower strip, the blocked periods get even longer, practically resulting in ventricular standstill. With such persisting absence of AV conduction, normally one would expect a ventricular ectopic focus to take over. This however, did not happen here.
Conclusively, this is atrial flutter with a high-degree atrioventricular block and intermittent episodes ventricular standstill. The patophysiology behind this could be AV-node tissue degeneration over time, leading to progressively increasing level of block.
December 16, 2009
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Patient: 75 y/o male. Medical history and anamnesis unknown. Experienced several Adams-Stokes episodes and his wife called EMS. This is a prehospital 12 lead from the LP12.
ECG description:
- No P-QRS relationship. Independent pacemakers.
- Atrial rate is 125 bpm. Ventricular rate is close to zero.
- No escape rhythm present
- P axis is normal at 60 degrees
Discussion:
This is ventricular standstill. The underlying rhythm is sinus tachycardia at 125 bpm, but there is complete failure of the impulses to reach the ventricles. The first QRS complex is of junctional origin, the second is from the ventricles, probably the right ventricle. Unfortunately, this 6 second recording does not tell whether this is an escape rhythm or just single beats.
October 3, 2009
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Patient/anamnesis: n/a
ECG interpretation/discussion: This ECG is a printout from a telemetry station, derived from a 5 lead patient monitoring. So, what have we here? The underlying rhythm is sinoatrial, but both PR and RR interval varies. Remember, Wenckebach is not the name of a certain type of block, but rather a type of conduction. This is often misunderstood, as Second Degree AV Block Type 1 or Mobitz 1 is also often labelled Wenckebach block. A more precise term would be Wenckebach periodity, phenomenon, conduction. Wenckebach conduction is usually considered benign and can be recognized by the following criteria:
1) PR interval is progressively prolonged until a P wave is blocked
2) The shortest PR interval is the one immediately following the dropped beat. The longest PR interval is the one immediately before the dropped beat. The incremental change in PR interval is in the beginning of the Wenckebach cycle, thus between the first and second PR interval in a sequence.
3) The RR intervals progressively shorten until a QRS is ‘dropped’ due to the non-conducted atrial/sinoatrial impulse.
Now, looking at this ECG, the two first beats are at the end of a Wenckebach cycle. After the second QRS a non-conducted P wave occurs. The following beat is wide and bizarre and is a ventricular escape beat that occurs due to the long preceding pause. After the escape beat, a new Wenckebach cycle starts. The PR interval lengthens until a P wave is blocked. After this pause, a narrow QRS is preceded by a P wave with a very, very short PR interval. This is a junctional escape beat. Then, the Wenckebach cycle restarts.
When counting P waves and QRS complexes in the cycles, we’ll see that for every three QRS complexes there are four P waves, since one of the QRS complexes gets dropped repeatedly. This gives a 4:3 atrioventricular (AV) ratio, which is also called 4:3 conduction.
What a beauty! Thanks to my colleague and fellow ECG-dork for bringing me this rare gem!
September 6, 2009
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Patient: n/a
ECG description:
- Sinus tachycardia
- Supraventricular bigemeny
- One premature ventricular contraction
Discussion:
There is a baseline sinus tachycardia with a PR interval of 130ms, regularly interrupted by premature atrial contractions (PAC). Each PAC depolarizes the atria and resets the SA node, causing a change in automaticity and a noncompensatory extrasystolic pause. Judging by the PR interval as well as P axis and morphology of the premature beats, the ectopic pacemaker is atrial. The ectopic PR interval is 130ms, and it is plausible to think that the ectopic pacemaker is located near the SA node. The P wave axis is ca. 30 degrees, and the ectopic P wave axis is ca. 60 degrees, which means that the atria are depolarized anterogradely and in almost the same direction as from the SA node. QRS axis and morphology is slightly different in the QRS complex following the first premature beat and the second and third. Looking closely, we can see that P wave axis and morphology slightly differs from the first PAC to the next two. The PR interval however is the same. This could be due to multifocality, but since the PR interval is quite similar, the two foci must be very close to each other. After the third bigeminal beat, a broad QRS occurs. In spite of the aberrantly looking RBBB-like morphology, this is most likely a premature ventricular contraction (PVC). If this was aberrancy, it would be due a refractory right bundle branch that couldn’t cope with the rapid changes in automaticity caused by the PAC’s. However, the coupling interval before the broad complex is similar to the other coupling intervals, and this demonstrates that the RBB in fact handles the rapid changes in automaticity quite well. In the precordial leads, we can see a P wave following the PVC, suggesting that the atrias have been depolarized retrogradely from the PVC.
July 1, 2009
The patient is an 80 y/o woman with known sick sinus syndrome, aortic sclerosis, aortic valve insufficiency, mitral valve insufficiency, tricuspidal valve insufficiency and left ventricular hypertrophy.
About the sick sinus syndrome and the tachy-brady syndrome
There are two types of Sick Sinus Syndrome (SSS): one with and one without associated tachyarrhythmias. SSS is due to many mechanisms related to SA-nodal failure, and in many patients with the syndrome more than one of the mechanisms are present. The most common mechanisms for SSS are severe, persistent sinus bradycardia, sinus arrest, both brief and sustained, with or without initiation of escape pacemakers, sometimes resulting in sustained asystole. Both Stokes-Adams attacks and sudden death is seen with SSS. When SSS is associated with tachyarrhytmhias, this is called the tachy-brady syndrome. Tachy-brady syndrome occurs in more than half of the patients with SSS.¹ The tachy-brady syndrome itself is not a specific condition, but more of a mixture of combinations of arrhythmias. I find it confusing that even the most profilic authors on this subject, as both Marriott² and Chou¹, tend to disagree on whether SSS should be considered part of the tachy-brady syndrome or vice versa. However, there seems to be consistency upon the fact that SSS can occur in two forms, with our without the associated tachycardias. Furthermore the tachy-brady syndrome is usually described as the condition where a tachycardia mechanism is directly associated with the mechanism of a bradycardia or the other way around. One author³ also differentiates between a tachy-brady syndrome and a brady-tachy syndrome, depending on what mechanism that initiates the next.
This series of telemetry strips from the patient described above, show the tachy-brady syndrome in action, manifested by a large and complex cascade of arrhythmic events. Note that there is a baseline first degree AV block at approximately 260 ms.
Note that each strip is not an exact continuation of the strip before it, meaning that i.e. strip number 2 can repeat some of the events in strip 1.
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Top strip: After 4 cycles of sinus bradycardia (43 bpm), atrial flutter occurs. The atrial rate is approximately 260 bpm, and 2:1 AV conduction occurs, resulting in a ventricular rate of 130 bpm. There are F waves (flutter waves) superimposed on each T wave.
Middle strip: Note that this strip is not an exact continuation of strip 1. The first 12 beats are the same. It shows however the atrial flutter persisting with the same AV ratio for several seconds.
Bottom strip: After a while, 4:1 conduction occurs for one cycle. The next cycle is interrupted by a PVC triplet, or a short run of ventricular tachycardia (VT). After the ventricular triplet, the AV node alternates with 2:1 and 3:1 conduction.
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Top strip: Atrial flutter still persists, while 2:1, 3:1 and 4:1 AV conduction occurs successively, before a four beat salvo of premature ventricular contractions occur. Such a salvo would also be considered non-sustained ventricular tachycardia. Following the salvo, AV ratio continues to vary and also with higher degrees of block. 2:1, 3:1 4:1 and 5:1 AV block occurs successively towards the end of the strip.
Middle strip: This strip is almost a repetition of the top strip, and can be ignored.
Bottom strip: Here we can see that even higher degree of AV block occurs, with AV ratio as high as 6:1 before progressively decreasing again.
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Top strip: This strip is recorded at 50mm/s, and shows the baseline atrial flutter being conducted with high degrees of AV block, and interrupted by a 5-beat run of ventricular tachycardia at 140 bpm.
Middle strip: Various degrees of AV block are seen throughout the strip. The deep, negative deflection towards the end is due to a loose electrode.
Bottom strip: AV block continues to vary, here mostly between a 2:1 and 3:1 ratio.
¹ Surawicz, Borys, Chou’s electrocardiography in clinical practice. Philadelphia: Saunders Elsevier, 2006:336-343, 6th edition.
² Wagner, Galen S., Marriott’s Practical Electrocardiography. Philadelphia: Lippincott Williams & Wilkins, 396-404, 10th edition
³ Sandøe, Erik and Bjarne Sigurd, Klinisk Elektrokardiografi. Bingen: Publishing Partners Verlag GmbH, 326-331, 1st edition.
June 18, 2009
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Patient: Woman, 82 y/o with permanent atrial fibrillation. Accidental digitalis intoxication. Serum digoxin level when arriving in the ER is 6.6 ng/ml. General fatigue, but no recent history of syncopal episodes.
ECG description:
- Irregular, narrow QRS bradycardia at approx. 35 bpm
- Atrial fibrillation with slow ventricular response
- Normal axis at ca. 60 degrees
- Prominent U waves, best seen in leads V2 -V3
- Cohn effect: ST segment depression and flattened T wave in leads V4-V6
- Poor R wave progression
- Low amplitude in limb leads
- Baseline noise artefact
Discussion: This 12 lead ECG displays atrial fibrillation with slow ventricular response. There is a high degree of AV block, resulting in a bradycardic rate at ca 35 bpm (50 mm/s). The axis is in the normal quadrant and at ca. 60 degrees. Limb leads show T wave flattening, and there is perhaps a slight ST segment depression visible in leads II and AVF. There is a quite prominent U wave. Normally, the U wave is best appreciated in the lateral precordial leads (V5-V6). Here however, it is seen in leads V2 and V3. The classic ST segment morphology induced by digitalis both at therapeutic and toxic serum levels, is the “coved” or “scooped”, or sometimes referred to as “bowl shaped” ST segment depression. It is sometimes described as if the ST segment has been dragged downwards from a point at the middle of the segment. Digitalis intoxications may however, manifest with or without the classic morphology even at high serum levels. The classic digitalis effect on the ST segment is sometimes called the Cohn Effect, named after Alfred E. Cohn, the American cardiologist, for his early 1900-century studies on the effect of digitalis on T wave morphology. It is generally recognized by ST segment depression together with T wave flattening in the same lead. Although this ECG lacks the coving ST segment, the Cohn effect is present in leads V4-V6.
Overall, digitalis has a positiv inotropic effect and a negative chronotropic effect. The negative chronotropy is due to both decreased automaticity of the SA node as well as prolongation of the refractory period of the AV nodal tissue, thus inducing higher degrees of AV block. It also increases AV nodal automaticity which often results in for instance accelerated junctional rhytm and junctional extrasystolia.
This ECG is in the low bradycardic range at around 35 bpm, which is due to the high serum levels of digoxin. Different AV ratios can occur, but 2:1 is rare. With second degree AV blocks, Wenckebach conduction is common. In this ECG it’s impossible to determine the AV ratio, due to atrial fibrillation, and one can only conclude that it is varying. Following is a continous rhythm strip (25 mm/s) of the patient that was obtained 10 minutes later, showing the development of higher degrees of AV block, resulting in long bradycardic cycles.
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Note the long, asystolic pauses. The first and third cycles are so long (>2 seconds) that ventricular escape occurs.
June 18, 2009
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Patient: Woman, 51 y/o. Mitral valve replacement 21 years ago. Known paroxysmal atrial fibrillation. Presents in the ER with nausea, pale skin, mild diaphoresis, palpitations and diffuse chest pain.
Prehospital ECG:
- Supraventricular tachycardia
- Ventricular rate is ca. 120 bpm
- Normal axis at ca. 10°
- Atrial activity best visible in lead V1, showing P waves with a slightly varying and prolonged PR interval.
- Several P waves superimposed and partially hidden in T waves
- Pseudo R waves in lead V1
Interpretation: This faxed ECG shows a supraventricular tachycardia, but right precordial lead V1 shows clear atrial activity. The small, peaked P waves with a slightly changing and prolonged PR interval suggests atrial ectopy. Ectopic Atrial Tachycardia rarely occurs with 1:1 ratio, as the AV node usually blocks half or more of the impulses. A common AV block ratio is 2:1. With a ventricular rate of 120 bpm, a 2:1 AV block would indicate an atrial rate of 240 bpm. This would be a typical atrial rate for ectopic atrial tachycardia. Using a ruler or a caliper and measuring from one of the visible P waves here, we will see exactly that: P waves appear at a rate of 240 bpm. The most visible P waves are right after or superimposed on T waves, and the others are hidden in or appearing right after each QRS, creating what looks like a small S wave, a pseudo S wave.
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To confirm the diagnosis, carotid pressure is applied while a rhythm strip is recorded. Paper speed is set to 50 mm/s in order to discern P waves more easily. When pressure is applied, a larger AV block is induced and 3:1 periods occur intermittently. During these blocks, clearly discernable P waves are seen in the right precordial leads. The P waves show atrial ectopic activity at a rate of 240 bpm, just as we suspected from the previous ECG. By marching out the P waves with a caliper, we’ll see that every other P wave gets completely or partially hidden in the QRS complexes when the ratio changes back to 2:1.
May 17, 2009
This case displays the a relatively young, male patient with a recent myocardial infarction who developes junctional tachycardia. Three 12 lead ECGs are presented: One that is 9 days prior to this admittance, one that is obtained on scene by EMS and finally the ECG obtained in on arrival in the ER. The three ECGs are compared to obtain the correct diagnosis.
Patient: Male, 45 y/o. Non-smoker, non-drinker. Diabetes Mellitus type I with early stage retinopathy. Previous anterior infarction (two months prior to this admittance), followed by PCI to the LAD. Now presented in the ER with minor pressing chest pain. The pain occured when he was bicycling home from work. Having had a previous MI he immediately called EMS, who arrived quickly and recorded a 12 lead ECG. EMS adminstered 0.4 mg Nitro sl and 2.5 mg Morphine iv, which relieved the patient of his pain. He was transported to the hospital for blood tests and a check-up. On arrival in the ER he was pain free, with no dyspnea, normal aand dry skin. Vital stats on initial assessment were BP 135/85, regular pulse, RF 16/min, SpO2 97% with O2 2 ltr/min.
This is the 12 lead ECG (LP12) that was obtained by EMS:
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The ECG is at 50 mm/s and shows:
- a regular, narrow complex bradycardia at 46 bpm
- no P waves
- left axis deviation (LAD)
- Left Anterior Fascicle Block
- poor R wave progression (PRWP); late precordial transition zone: lead V6.
- normal ST-T segments
- minor baseline noise
Intepretation:
RHYTHM: This narrow, complex bradycardia has no visible P waves. The rhythm is regular and in the bradycardic range. What is the rhythm here? Narrow QRS complexes tell us that the rhythm is supraventricular, and added up with the regularity of the RR intervals, one should immediately suspect a junctional rhythm. The ventricles are paced at 46 bpm, which is slow enough to call this a bradycardia. Every myocardial cell has the ability to pace the heart, and each type of cell has its own intrisic rate that is slower than the type of cell preceding it. The fastest pacer is the SA node. Junctional and AV nodal cells pace in the range of ca. 45-50 bpm. Which means that this rate of 46 bpm also supports the theory of this being a junctional rhythm. As with all supraventricular impulses, the atria is usually depolarized. With junctional automaticity, the atria is normally depolarized in a retrograde fashion. With junctional rhythms, the P wave is therefore often found right after the QRS complex or in the following T wave, unless retrograde conduction is delayed, creating a prolonged RP interval. If visible, the P wave occuring from the retrograde atrial activation should be inverted in the inferior leads II, III and aVF.
R WAVE PROGRESSION: This patient’s previous anterior MI can be seen from the poor R wave progression in the precordial leads. To determine the R wave progression, one needs to identify the transition zone. This is the lead with equal R and S wave voltage (R/S=1). Normal R wave progression has an increasing R wave amplitude across the precordial leads, and a transition zone in V2, V3 or V4, where the voltage decreases again towards V6. Poor R wave progression is defined when the transition is late and doesn’t occur until V5 or V6. In this ECG the transition occurs in lead V6, indicating loss of myocardial tissue. Note that abnormal R waves and R wave progression can occur due to several other reasons, as for instance misplaced leads. However in this case, the PRWP correlates with the patient’s previous anterior MI.
Cherchez le P!
Again, those famous words by Dr. Marriott become useful. In this ECG the sinus node seems to be completely silent. There are no obvious P waves preceding any of the QRS complexes. By closely examining the QRS morphology in the right precordial leads V1 and V2, we find a small terminal R wave. These are actually pseudo R waves, and are called so because they are not really R waves, but instead retrograde P waves that occur right after the QRS complex.
Let’s compare to a previous ECG, taken 9 days prior to the first one:
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- Sinus rhythm at 76 bpm
- Left Axis Deviation (LAD)
- Left Anterior Fascicle Block
- First Degree Atrioventricular Block (1AVB); the PR interval is 220 ms
- One non-conducted premature atrial contraction (PAC); best seen in lead V2 as a small bump on the initial part of the T wave after the third QRS complex from the left)
- Poor R Wave Progression (PRWP); late transition zone – the transition occurs in V6.
First of all, the most striking observation here, is that this ECG shows a normal sinus rhythm. This tells us that this patient’s heart was had a working sinoatrial node just 9 days ago. However, there is a 1AVB present, which could be a sign of AV nodal disease.
This next ECG is taken on arrival in the ER, only 50 minutes later than the prehospital ECG:
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As we can see, the rate has increased. The rhythm is still junctional, but now pacing at a rate faster than the normal intrinsic rate of AV nodal and junctional pacemaker cells. The rate is 100bpm, making this an accelerated junctional rhythm (AJR). The retrograde atrial activation is still seen as pseudo R waves in lead V1.
March 26, 2009
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Patient: Woman, 70 y/o. Congestive Heart Failure. Using digitalis.
ECG description:
- Narrow complex tachycardia of supraventricular origin.
- Variable ventricular rate. Rate varies from 73-105 bpm.
- Right Axis Deviation. Cardiac axis is at approx. 150°
- Multiple P’ waves. Atrial rate is 210 bpm.
- Varying AV Block. P:QRS ratio ranging from 1:1 to 3:1.
- Ectopic P’ waves, inverted in inferior leads II, III, aVF. P waves superimposed on QRS complexes.
- Prominent Q waves in inferior leads, II, III aVF.
- T wave inversion in inferior leads, II, III, aVF
ECG comments: This EKG shows an Ectopic Atrial Tachycardia (EAT) with variable degree of AV Conduction, and was in the clinical setting mistaken for atrial flutter when the patient was presented in the ER. A common mistake to make, as atrial flutter is probably the arrhythmia that resembles EAT the most electrocardiographically. Atrial flutter is a common differential diagnosis with EAT, but making the wrong diagnosis here can however, be dangerous for the patient. The pitfall is that paradoxically, atrial flutter is treated with digitalis, which again induces EAT. Which means that if EAT is being mistakenly treated with digitalis, the arrhythmia will be sustained, as well as the degree of AV block could be increased. This will be like adding fuel to a fire. Untreated EAT with block can at some point compromise the patient’s cardiac output and result in hemodynamic unstability. The treatment for EAT is, of course to remove the digitalis intoxication.
Differentiating Ectopic Atrial Tachycardia and Atrial Flutter
The reason that EAT is often mistaken for atrial flutter, is because of the multiple P waves. Depending on their axis and morphology, they can for the untrained eye easily resemble flutter waves (F waves). Also, if one suspects an atypical flutter pattern, one might think that the P waves are due to flutter activity. However, the key is to understand the electrophysiology behind the two mechanisms and how they will appear on a surface EKG. If you understand the underlying electrophysiologic mechanisms of atrial flutter, differentiating it on a surface EKG is much easier. Also, by examining both the P waves and the baseline of the different leads, the correct diagnosis will be easily within reach in most cases.
Atrial Flutter
- Is characterized by a rapid and regular atrial rhythm at rates from 250 to 400 bpm.
- Due to the macroreentry mechanism of atrial flutter, where an ectopic impulse travels counterclockwisely in a circular fashion usually within the right atria, flutter waves are created on the EKG. When the impulse has travelled a full circle, it reactivates the same focus again, creating a reentry loop mechanism. Thus, where one F-wave ends, the next one arises immediately. Several F waves together makes out the hallmark saw tooth baseline.
- Flutter waves (F waves) and the saw tooth pattern are best seen in the inferior leads, II, III and aVF. Sometimes, F waves are more clearly visible in lead V1.
- Seldom coexist with ectopic atrial tachycardia in the same patient
Ectopic Atrial Tachycardia with block
- Is characterized by a rapid and regular atrial rhythm at rates from 150 to 250 bpm
- Has abnormal P (or P’) waves whose morphology is different from that of the sinus P waves. P waves are often inverted in inferior leads (II, III, aVF) if the ectopic focus sits distally in the atria.
- Has isoelectric intervals between P waves in all leads.
- When atrial rates become fast, the AV Node usually blocks signals. EAT never occurs with First Degree AV Block. Always presents with Second Degree or Third Degree AV Blocks. Wenckebach conduction can also occur.
- P waves are often difficult to spot as they are often small and dysmorph, and often get buried in or superimposed on the QRS complex. Lead II is often difficult to use, while lead V1 is often a good lead for discerning P waves.
- Often occurs due to digitalis intoxication
Cherchez le P!
The above are the famous words by EKG master Henry J. L. Marriott, and is french for “Look for the P!”. What Marriott meant, was that finding and evaluating the P waves is the key to understanding and diagnosing arrhythmias. Marriott especially pointed out that one must look for P waves buried in T waves. In both premature contractions, like for instance a PAC, and in other conditions, P waves can get buried in both the preceding T wave, in the QRS and practically anywhere. And as we will see with this EKG, spotting P waves is what pinpoints the diagnosis.
The rhythm is obviously supraventricular, as QRS complexes are within the normal range (<120 ms). There are multiple, small P waves before many of the QRS complexes. The P:QRS ratio varies from 3:1 in the longest cycles to what seems like 1:1 in the shortest cycles. However, the latter is actually 2:1. When examining the QRS complexes, there are P waves buried in the QRS complex. The buried P waves appear at the end of the QRS, and are best seen in leads V2-V5, as they create a pseudo S wave at the end of each QRS. By marching out the P waves with a caliper, the buried P waves are easy to spot. With this in mind, and knowing that First Degree AV Block doesn’t occur with EAT, we will conclude that where AV block ratio seemed to be 1:1, the block is really 2:1. This means that in those cycles, there are actually two P waves for each QRS, but the second P wave is buried in the QRS itself. These are however, not sinus P waves. They are deflections from an ectopic atrial focus, and should therefore be referred to as P’ waves, which is the correct labelling for ectopic P waves.
By measuring the P’P’ interval, the atrial rate is constant and regular at 210 bpm. In the 2:1 block cycles, the ventricular rate is 105 bpm. The ventricular rate is half the atrial rate, which correlates with a 2:1 block. Now, remembering what Dr. Marriott preached, when examining the T waves, there are clearly P waves buried in their humps. This is best seen in lead V3, where T wave morphology changes throughout the lead. The extra peaks and bumps on the T waves are actually buried P’ waves. If these were not observed, this rhythm could be mistaken for an AV Nodal Reentry Tachycardia, as there would be no P waves preceding the QRS, with seemingly retrograd P waves shortly after ventricular depolarization. Also, you will note that:
- The baseline is perfectly isoelectric between each P’ wave, ruling out the macro reentry impulse rotation mechanism of atrial flutter.
- In inferior leads II, III and aVF, the P’ waves are inverted as the P wave axis is shifted superiorly. This indicates a low atrial focus and is a common sign of atrial ectopy. This again rules out atrial flutter, which would produce F-waves in the same leads.
- Unlike MAT (Multifocal Atrial Tachycardia), there are not multiple ectopic foci here. The P wave configuration is constant and unimorph throughout the leads.
February 3, 2009
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Patient: n/a
ECG description:
- Sinus rhythm with varied rate: 75-130 bpm
- Premature Atrial Contractions (PAC) presenting in couplets
- Left Axis Deviation (LAD). Cardiac Axis is deviated leftwards and superiorly at approx. 90°
- Left Anterior Fascicular Block (LAFB) due to LAD, deep S in III, no sign of LVH or MI
- Low Voltage in Limb Leads
- Poor R Wave Progression (PRWP)
Atrial Couplets, PACs and P waves
After one sinus cycle, the rhythm is interrupted by a PAC (complex no. 3 from the left). The change in P wave axis and morhpology of this complex suggests ectopy. The P’ wave is inverted in leads II, III and aVF, suggesting that the ectopic impulse originates in the left atria, spreading in a retrograde fashion. Determining by the PR interval, which is 100 ms, the ectopic pacemaker is atrial and not junctional, and sits closer to the AV Node than the SA Node.
The PAC is immediately followed by a new PAC, creating an atrial couplet. This second PAC seems to originate from another focus, as there is a change in P’ wave axis and configuration. The PR interval of this PAC is 110ms, and the P’ waves are upright in the inferior leads, suggesting that it spreads inferiorly and towards the left. The second PAC is followed by two sinus cycles, which is then followed by another PAC couplet. The PACs in this couplet seem to originate from the same ectopic foci as in the first couplet, although there is a variation in coupling interval length.
Atrial couplets can be benign, but are less common in healthy hearts, and should increase suspicion towards onset of atrial fibrillation. Ultimately, one would prefer to print a longer rhythm strip at this point, to see the phenomenon over a longer time interval. Unfortunately this is not available for this particular case.
The Postextrasystolic Pause
With supraventricular premature impulses, the dominant automaticity focus (normally the SA Node, as in this case) is usually reset by the premature impulse. The supraventricular impulse usually activates the whole atria and thereby also the SA Node. The early activation of the SA Node interrupts the pacing function of the node, and causes a delay in impulse generation. The next impulse will then be slightly delayed, causing the following RR interval to be prolonged. This is called a noncompensatory pause. If the SA Node is not reset, then its pacing function will not be disturbed, and the following RR interval will be an exact multiple of the normal interval, resulting in a compensatory pause.
PACs usually present with non-compensatory pauses, as ectopic atrial impulses will usually activate the whole atria, including the SA Node, and thereby interrupting the sinus pacing activity. In this EKG, the pause after the first PAC is interrupted early by another ectopic impulse, so this pause cannot be determined. The second PAC however (complex no. 4 from the left) is followed by a postextrasystolic pause that is prolonged, but still not an exact multiple of the normal sinus cycle length. This is a non-compensatory pause, which tells us that the SA Node has been reset. This helps to establish and diagnose an atrial origin for the ectopic beats.
January 30, 2009
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